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The Effects of Daily Repeated Magnetic Field on S-Nitroso-N-acetyl-DL penicillamine Induced Hyperalgesia

Yıl 2014, Cilt: 36 Sayı: 3, 310 - 319, 30.09.2014
https://doi.org/10.7197/cmj.v36i3.1008002547

Öz

Abstract

Aim. The treatment of pain has been one of the most important objectives of medicine. We aimed to investigate antinociceptive effects and mechanisms of magnetic field (MF) on the hyperalgesia produced by S-Nitroso N-acetyl penicillamine (SNAP). Method. Study has been made in two sections. In the first section, rats were divided four groups (six in each). The first group was determined as sham group and administrated 0.3 mL, 0.9% NaCl intraperitoneally (i.p) before assessing tail flick latencies (TFLs) (Sham group). In the second group, 2 mg/kg SNAP administrated i.p. and TFLs were assessed at the same time points with first group (SNAP group). In the third group, rats were repeatedly exposed to MF for 6 consecutive days (MF group). In the fourth group, SNAP was administrated i.p everyday shortly before MF exposure (SNAP+MF group). In the second section, animals divided to the same groups with the first section. Same procedures have been performed with the first section groups and blood samples were collected to determine plasma levels of β-endorphin and substance P. Results. SNAP (2 mg/kg) produced hyperalgesic effect with i.p. administration. MF application (5 mT and 165 min per day) produced a strong antinociception in Days 3 and 4. Tail flick values of SNAP+MF in Days 3 and 4 were found to be significantly low as compared to MF and Sham groups. In SNAP group, substance P levels were found to be significantly high. Plasma β-endorphin levels in MF and SNAP+MF groups were significantly high as compared to the Sham group. Conclusion. MF may be an alternative antinociceptive approach for pain treatment. There is need for further studies to overcome the tolerance to antinociceptive effects of MF.

Keywords: Hyperalgesia, magnetic field, snap, substance p, β-endorphin, tail flick

 

Özet

Amaç. Ağrı tedavisi tıbbın en önemli hedeflerinden biridir. Bu araştırmada manyetik alan uygulamasının S-Nitroso N-acetyl penicillamine (SNAP) tarafından oluşturulan ağrı üzerindeki etkilerini ve etki mekanizmasını araştırmayı amaçladık. Yöntem. Çalışma iki kısım olacak şekilde tasarlandı. Birindi kısımda hayvanlar her birinde altı hayvan olacak şekilde 4 gruba bölündü. Birinci grup sham grubu olarak belirlendi ve bu hayvanlara 0,3 mL %0,9 NaCl tail flick latensleri ölçülmeden once uygulandı. İkinci gruba (SNAP grubu) 2 mg/kg SNAP i.p. olarak enjekte edildi ve sham grubu ile aynı zaman noktalarında tail flick ölçümleri yapıldı. Üçüncü grup (MF grubu) tekrarlayan altı gün boyunca manyetik alana maruz bırakıldı. Dördüncü grupta (SNAP+MF) hayvanlara manyetik alan uygulaması yapılmadan hemen önce 2 mg/kg SNAP i.p. olarak uygulandı. Çalışmanın ikinci kısmında ratlardan kan örnekleri alınarak kanlarında supstance p ve B-endorfin seviyelerine ELISA yöntemi ile bakıldı. Bulgular. SNAP (2 mg/kg) anlamlı bir hiperaljezi meydana getirerek tail flick latenleslerini kısalttı. Manyeteik alan uygulaması (5 mT ve 165 dakika/gün) özellikle 3. ve 4. günlerde anlamlı bir analjezi meydana getirdi. SNAP grubunda substance p seviyeleri yüksek bulunurken, manyetik alan grubunda B-endorfin seviyelerinin yüksek olduğu tespit edildi. Sonuç. Bu sonuçlar manyetik alan uygulamasının ağrı tedavisinde alternatif bir yaklaşım olabileceğini göstermektedir. Fakat bu yöntemin kullanılabilmesi için gelişen toleransın üstesinden gelmenin yollarının bulunması ve bunun içinde ileri araştırmalara gereksinim vardır.

Anahtar sözcükler: Hiperaljezi, manyetik alan, snap, p maddesi, β-endorfin, tail flick

Kaynakça

  • IASP International Association for the Study of Pain. IASP Pain Terminology [IASP web site]. November 9, 2004. http://www.iasp-pain.org/terms-p.html. (Erişim tarihi: 12.09.2014).
  • Smith BH, Elliott AM, Chambers WA, Cairns SW, Hannaford PC, Penny K. The impact of chronic pain in the community. Fam Pract 2001; 18: 292-9.
  • Gureje O, Von Korff M, Simon GE, Gater R. Persistent pain and well-being: A World Health Organization Study in Primary Care. JAMA 1998; 280: 147-51.
  • Aimar P, Pasti L, Carmignoto G, Merighi A. Nitric Oxide-Producing Islet Cells Modulate the Release of Sensory Neuropeptides in the Rat Substantia Gelatinosa. Jour Neurosci 1998; 18: 10375-88.
  • Burlet S, Cespuglio R, Voltammetric detection of nitric oxide (NO) in the rat brain: Its variations throughout the sleep-wake cycle. Neurosci Lett 1997; 226: 131Luo ZD, Cizkova D. The role of nitric oxide in nociception. Curr Rev Pain 2000; 4: 459-66.
  • Saito S, Kidd GJ, Trapp BD, Dawson TM, Bredt DS, Wilson DA, Traystman RJ, Snyder SH, Hanley DF. Rat spinal cord neurons contain nitric oxide synthase. Neuroscience 1994; 59: 447-56.
  • Przewlocka B, Machelska H, Przewlocki R. Involvement of the nitric oxide pathway in nociceptive processes in the central nervous system in rats, Regul Pept 1997; 1: 75-6.
  • Hao JX, Xu XJ. Treatment of a chronic allodynia-like response in spinally injured rats: Effects of systemically administered nitric Nitric oxide directly activate calcium-dependent potassium chan- oxide synthase inhibitors. Pain 1996; 66: 313Yonehara N, Takemura M, Yoshimura M, Iwase K, Seo HG, Taniguchi N, Shigenaga Y. Nitric oxide in the rat spinal cord in Freund’s adjuvant-induced hyperalgesia, Jpn J Pharmacol 1997; 75: 327-35.
  • Holthusen H, Arndt JO. Nitric oxide evokes pain at nociceptors of the paravascular tissue and veins in humans. J Physiol 1995; 487: 253-8.
  • Holthusen H. Involvement of the NO/cyclic GMP pathway in bradykininevoked pain from veins in humans. Pain 1997; 69: 87-92.
  • Kitto, KF, Haley JE, Wilcox GL. Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse. Neurosci Lett 1992; 148: 1-5.
  • Meller ST, Dykstra C, Gebhart GF. Production of endogenous nitric oxide and activation of soluble guanylate cyclase are required for N-methyl-D-aspartateproduced facilitation of the nociceptive tail-flick reflex. Eur J Pharmacol 1992; 214: 93-6.
  • Meller ST, Pechman P.S, Gebhart G.F, Maves T.J. Nitric oxide mediates the thermal hyperalgesia produced in a model of neuropathic pain in the rat. Neuroscience 1992; 50: 7-10.
  • Coderre, TJ, Yashpal, K. Intracellular messengers contributing to persistent nociception and hyperalgesia induced by L-glutamate and substance P in the rat formalin pain model. Eur J Neurosci 1994; 6: 1328-34.
  • Durate ID, Lorenzetti BB, Ferreira SH. Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathway. Eur J Pharmacol 1990; 186: 289-93.
  • Tonussi CR, Ferreira SH. Mechanism of diclofenac analgesia: Direct blockade of inflammatory sensitization. Eur J Pharmacol 1994; 251: 173-9.
  • Cunha FQ, Teixera MM, Ferreira SH. Br J Pharm 1999; 127: 671-8.
  • Panagopoulos DJ, Karabarbounis A, Margaritis LH. Mechanism for action of electromagnetic fields on cells. Biochem Biophys Res Commun 2002; 298: 95
  • Grassi C, D’Ascenzo M, Torsello A, Martinotti G,Wolf F, Cittadini A, Azzena GB. Effects of 50 Hz electromagnetic fields on voltage-gated Ca+2 channels and their role in modulation of neuroendocrine cell proliferation and death. Cell Calcium 2004; 35: 307-15.
  • Sartucci F, Bonfiglio L, Del Seppia C, Luschi P, Ghione S, Murri L, Papi F. Changes in pain perception and pain-related somatosensory evoked potentials in humans produced by exposure to oscillating magnetic fields. Brain Res. 1997; 769: 362-6.
  • Martin LJ, Persinger MA. Thermal analgesia induced by 30-min exposure to 1 mT burst-firing magnetic fields is strongly enhanced in a dose-dependent manner by the α2 agonist clonidine in rats. Neurosci Lett 2004; 366: 226-9.
  • Carpenter DO, Ayrapetyan S. Biological Effects of Electric and Magnetic Fields, Academic Press, San Diego, CA 1994; 1: 369.
  • Meller ST, Gebhart GF. Nitric oxide (NO) and nociceptive processing in the spinal cord. Pain 1993; 52: 127-36.
  • Lam HH, Hanley DF, Trapp BD, Saito S, Raja S, Dawson TM, Yamaguchi H. Induction of spinal cord neuronal nitric oxide synthase (NOS) after formalin injection in the rat hind paw. Neurosci Lett 1996; 210: 201-4.
  • Garry MG, Richardson JD, Hargreaves KM. Carrageenan induced inflammation alters the content of i-cGMP and i-cAMP in the dorsal horn of the spinal cord. Brain Res 1994; 646: 135-9.
  • Kavaliers M, Ossenkopp KP. Tolerance to morphine-induced analgesia in mice: Magnetic fields function as environmental specific cues and reduce tolerance development. Life Science 1985; 37: 1125-35.
  • Kavaliers M, Ossenkopp KP. Repeated naloxone treatments and exposures to weak 60 Hz magnetic fields have ‘analgesic’ effects in snail. Brain Research 1993; 620: 159-62.
  • Bao X, Shi Y, Huo X, Song T. A Possible involvement of β-endorphin, substance P, and Serotonin in rat analgesia induced by extremely low frequency Magnetic Field. Bioelectromagnetics 2006; 27: 467-72.
  • Tiffany ST, Maude-Griffin PM. Tolerance to morphine in the rat: Associative and non-associative effects. Behav Neurosci 1988; 102: 434-43.
  • Rosen A, Zhang YX, Lund I, Lundeberg T, Yu LC. Substance P microinjected into the periaqueductal gray matter induces antinociception and is released following morphine administration. Brain Res 2004; 1001: 87-94.
  • Iversen LL. Substance P. Brit Med Bull 1982; 37: 277-82.
  • Nagy JI, Van Der Kooy D. Effects on neanatal capsaicin treatment on nociceptive thresholds in the rat. J Neurosci 1983; 3: 1145-50.
  • Randic M, Miletic V. Effect of substance P in cat dorsal horn neurones activated by noxious stimuli. Brain Res 1977; 128: 164-9.
  • Yaksh TL, Farb DH, Leeman SE. Intrathecal capsaicin depletes substance P in the rat spinal cord and produces prolonged thermal analgesia. Science 1979; 206: 481Terman GW, Shavit Y, Lewis JW, Cannon JT, Liebeskind JC. Intrinsic mechanisms of pain inhibition: Activation by stress. Science 1984; 226: 1270-2.
  • Basbaum AI, Fields HL, Endogenous pain control systems: Brainstem spinal pathways and endorphin circuitry. Annu Rev Neurosci 1984; 7: 309-38.
  • Panerei IE, Martini A, Sacdrhdte P, Mantegazza P. K-Receptor antagonist reverses “non-opioid” stress-induced analgesia. Brain Res 1984; 304: 153-6.
  • Millan MJ, Millan MH, Pilcher CWT, CzJonkowski A, Herz A, Colpaert FC. Spinal cord dynorphin may modulate nociception via a K-opioid receptor in chronic arthritic rats. Brain Res 1985; 340: 156-9.
  • Millan MJ, Millan MH, Cztonkowski A, Hiillt V, Pilcher CWT, Herz A, Colpaert FC. A model of chronic pain in the rat: Response of multiple opioid systems to adjuvant-induced arthritis. J Neurosci 1986; 6: 899-906.
  • Millan MJ, Millan MH, Czkonkowski A, Pilcher CWT, Hiillt V, Colpaert FC, Herz A. Functional response of multiple opioid systems to chronic arthritic pain in the rat. Ann NY Acad Sci 1986; 467: 182-93.

Original research-Orijinal araştırma

Yıl 2014, Cilt: 36 Sayı: 3, 310 - 319, 30.09.2014
https://doi.org/10.7197/cmj.v36i3.1008002547

Öz

Amaç. Ağrı tedavisi tıbbın en önemli hedeflerinden biridir. Bu araştırmada manyetik alan uygulamasının S-Nitroso N-acetyl penicillamine (SNAP) tarafından oluşturulan ağrı üzerindeki etkilerini ve etki mekanizmasını araştırmayı amaçladık. Yöntem. Çalışma iki kısım olacak şekilde tasarlandı. Birindi kısımda hayvanlar her birinde altı hayvan olacak şekilde 4 gruba bölündü. Birinci grup sham grubu olarak belirlendi ve bu hayvanlara 0,3 mL %0,9 NaCl tail flick latensleri ölçülmeden once uygulandı. İkinci gruba (SNAP grubu) 2 mg/kg SNAP i.p. olarak enjekte edildi ve sham grubu ile aynı zaman noktalarında tail flick ölçümleri yapıldı. Üçüncü grup (MF grubu) tekrarlayan altı gün boyunca manyetik alana maruz bırakıldı. Dördüncü grupta (SNAP+MF) hayvanlara manyetik alan uygulaması yapılmadan hemen önce 2 mg/kg SNAP i.p. olarak uygulandı. Çalışmanın ikinci kısmında ratlardan kan örnekleri alınarak kanlarında supstance p ve B-endorfin seviyelerine ELISA yöntemi ile bakıldı. Bulgular. SNAP (2 mg/kg) anlamlı bir hiperaljezi meydana getirerek tail flick latenleslerini kısalttı. Manyeteik alan uygulaması (5 mT ve 165 dakika/gün) özellikle 3. ve 4. günlerde anlamlı bir analjezi meydana getirdi. SNAP grubunda substance p seviyeleri yüksek bulunurken, manyetik alan grubunda B-endorfin seviyelerinin yüksek olduğu tespit edildi. Sonuç. Bu sonuçlar manyetik alan uygulamasının ağrı tedavisinde alternatif bir yaklaşım olabileceğini göstermektedir. Fakat bu yöntemin kullanılabilmesi için gelişen toleransın üstesinden gelmenin yollarının bulunması ve bunun içinde ileri araştırmalara gereksinim vardır.

Kaynakça

  • IASP International Association for the Study of Pain. IASP Pain Terminology [IASP web site]. November 9, 2004. http://www.iasp-pain.org/terms-p.html. (Erişim tarihi: 12.09.2014).
  • Smith BH, Elliott AM, Chambers WA, Cairns SW, Hannaford PC, Penny K. The impact of chronic pain in the community. Fam Pract 2001; 18: 292-9.
  • Gureje O, Von Korff M, Simon GE, Gater R. Persistent pain and well-being: A World Health Organization Study in Primary Care. JAMA 1998; 280: 147-51.
  • Aimar P, Pasti L, Carmignoto G, Merighi A. Nitric Oxide-Producing Islet Cells Modulate the Release of Sensory Neuropeptides in the Rat Substantia Gelatinosa. Jour Neurosci 1998; 18: 10375-88.
  • Burlet S, Cespuglio R, Voltammetric detection of nitric oxide (NO) in the rat brain: Its variations throughout the sleep-wake cycle. Neurosci Lett 1997; 226: 131Luo ZD, Cizkova D. The role of nitric oxide in nociception. Curr Rev Pain 2000; 4: 459-66.
  • Saito S, Kidd GJ, Trapp BD, Dawson TM, Bredt DS, Wilson DA, Traystman RJ, Snyder SH, Hanley DF. Rat spinal cord neurons contain nitric oxide synthase. Neuroscience 1994; 59: 447-56.
  • Przewlocka B, Machelska H, Przewlocki R. Involvement of the nitric oxide pathway in nociceptive processes in the central nervous system in rats, Regul Pept 1997; 1: 75-6.
  • Hao JX, Xu XJ. Treatment of a chronic allodynia-like response in spinally injured rats: Effects of systemically administered nitric Nitric oxide directly activate calcium-dependent potassium chan- oxide synthase inhibitors. Pain 1996; 66: 313Yonehara N, Takemura M, Yoshimura M, Iwase K, Seo HG, Taniguchi N, Shigenaga Y. Nitric oxide in the rat spinal cord in Freund’s adjuvant-induced hyperalgesia, Jpn J Pharmacol 1997; 75: 327-35.
  • Holthusen H, Arndt JO. Nitric oxide evokes pain at nociceptors of the paravascular tissue and veins in humans. J Physiol 1995; 487: 253-8.
  • Holthusen H. Involvement of the NO/cyclic GMP pathway in bradykininevoked pain from veins in humans. Pain 1997; 69: 87-92.
  • Kitto, KF, Haley JE, Wilcox GL. Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse. Neurosci Lett 1992; 148: 1-5.
  • Meller ST, Dykstra C, Gebhart GF. Production of endogenous nitric oxide and activation of soluble guanylate cyclase are required for N-methyl-D-aspartateproduced facilitation of the nociceptive tail-flick reflex. Eur J Pharmacol 1992; 214: 93-6.
  • Meller ST, Pechman P.S, Gebhart G.F, Maves T.J. Nitric oxide mediates the thermal hyperalgesia produced in a model of neuropathic pain in the rat. Neuroscience 1992; 50: 7-10.
  • Coderre, TJ, Yashpal, K. Intracellular messengers contributing to persistent nociception and hyperalgesia induced by L-glutamate and substance P in the rat formalin pain model. Eur J Neurosci 1994; 6: 1328-34.
  • Durate ID, Lorenzetti BB, Ferreira SH. Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathway. Eur J Pharmacol 1990; 186: 289-93.
  • Tonussi CR, Ferreira SH. Mechanism of diclofenac analgesia: Direct blockade of inflammatory sensitization. Eur J Pharmacol 1994; 251: 173-9.
  • Cunha FQ, Teixera MM, Ferreira SH. Br J Pharm 1999; 127: 671-8.
  • Panagopoulos DJ, Karabarbounis A, Margaritis LH. Mechanism for action of electromagnetic fields on cells. Biochem Biophys Res Commun 2002; 298: 95
  • Grassi C, D’Ascenzo M, Torsello A, Martinotti G,Wolf F, Cittadini A, Azzena GB. Effects of 50 Hz electromagnetic fields on voltage-gated Ca+2 channels and their role in modulation of neuroendocrine cell proliferation and death. Cell Calcium 2004; 35: 307-15.
  • Sartucci F, Bonfiglio L, Del Seppia C, Luschi P, Ghione S, Murri L, Papi F. Changes in pain perception and pain-related somatosensory evoked potentials in humans produced by exposure to oscillating magnetic fields. Brain Res. 1997; 769: 362-6.
  • Martin LJ, Persinger MA. Thermal analgesia induced by 30-min exposure to 1 mT burst-firing magnetic fields is strongly enhanced in a dose-dependent manner by the α2 agonist clonidine in rats. Neurosci Lett 2004; 366: 226-9.
  • Carpenter DO, Ayrapetyan S. Biological Effects of Electric and Magnetic Fields, Academic Press, San Diego, CA 1994; 1: 369.
  • Meller ST, Gebhart GF. Nitric oxide (NO) and nociceptive processing in the spinal cord. Pain 1993; 52: 127-36.
  • Lam HH, Hanley DF, Trapp BD, Saito S, Raja S, Dawson TM, Yamaguchi H. Induction of spinal cord neuronal nitric oxide synthase (NOS) after formalin injection in the rat hind paw. Neurosci Lett 1996; 210: 201-4.
  • Garry MG, Richardson JD, Hargreaves KM. Carrageenan induced inflammation alters the content of i-cGMP and i-cAMP in the dorsal horn of the spinal cord. Brain Res 1994; 646: 135-9.
  • Kavaliers M, Ossenkopp KP. Tolerance to morphine-induced analgesia in mice: Magnetic fields function as environmental specific cues and reduce tolerance development. Life Science 1985; 37: 1125-35.
  • Kavaliers M, Ossenkopp KP. Repeated naloxone treatments and exposures to weak 60 Hz magnetic fields have ‘analgesic’ effects in snail. Brain Research 1993; 620: 159-62.
  • Bao X, Shi Y, Huo X, Song T. A Possible involvement of β-endorphin, substance P, and Serotonin in rat analgesia induced by extremely low frequency Magnetic Field. Bioelectromagnetics 2006; 27: 467-72.
  • Tiffany ST, Maude-Griffin PM. Tolerance to morphine in the rat: Associative and non-associative effects. Behav Neurosci 1988; 102: 434-43.
  • Rosen A, Zhang YX, Lund I, Lundeberg T, Yu LC. Substance P microinjected into the periaqueductal gray matter induces antinociception and is released following morphine administration. Brain Res 2004; 1001: 87-94.
  • Iversen LL. Substance P. Brit Med Bull 1982; 37: 277-82.
  • Nagy JI, Van Der Kooy D. Effects on neanatal capsaicin treatment on nociceptive thresholds in the rat. J Neurosci 1983; 3: 1145-50.
  • Randic M, Miletic V. Effect of substance P in cat dorsal horn neurones activated by noxious stimuli. Brain Res 1977; 128: 164-9.
  • Yaksh TL, Farb DH, Leeman SE. Intrathecal capsaicin depletes substance P in the rat spinal cord and produces prolonged thermal analgesia. Science 1979; 206: 481Terman GW, Shavit Y, Lewis JW, Cannon JT, Liebeskind JC. Intrinsic mechanisms of pain inhibition: Activation by stress. Science 1984; 226: 1270-2.
  • Basbaum AI, Fields HL, Endogenous pain control systems: Brainstem spinal pathways and endorphin circuitry. Annu Rev Neurosci 1984; 7: 309-38.
  • Panerei IE, Martini A, Sacdrhdte P, Mantegazza P. K-Receptor antagonist reverses “non-opioid” stress-induced analgesia. Brain Res 1984; 304: 153-6.
  • Millan MJ, Millan MH, Pilcher CWT, CzJonkowski A, Herz A, Colpaert FC. Spinal cord dynorphin may modulate nociception via a K-opioid receptor in chronic arthritic rats. Brain Res 1985; 340: 156-9.
  • Millan MJ, Millan MH, Cztonkowski A, Hiillt V, Pilcher CWT, Herz A, Colpaert FC. A model of chronic pain in the rat: Response of multiple opioid systems to adjuvant-induced arthritis. J Neurosci 1986; 6: 899-906.
  • Millan MJ, Millan MH, Czkonkowski A, Pilcher CWT, Hiillt V, Colpaert FC, Herz A. Functional response of multiple opioid systems to chronic arthritic pain in the rat. Ann NY Acad Sci 1986; 467: 182-93.
Toplam 39 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Bölüm Temel Tıp Bilimleri Araştırma Yazıları
Yazarlar

Ahmet Altun

Mustafa Ergül

Ali Filiz

Mesut Parlak

Merve Ergül

Tijen Temiz

Yayımlanma Tarihi 30 Eylül 2014
Yayımlandığı Sayı Yıl 2014Cilt: 36 Sayı: 3

Kaynak Göster

AMA Altun A, Ergül M, Filiz A, Parlak M, Ergül M, Temiz T. The Effects of Daily Repeated Magnetic Field on S-Nitroso-N-acetyl-DL penicillamine Induced Hyperalgesia. CMJ. Eylül 2014;36(3):310-319. doi:10.7197/cmj.v36i3.1008002547